How do sigma factors help regulate gene expression during the transition to stationary phase?Sigma factors are transcriptional inhibitors, they stop transcription entirely so the bacteria don't wasteenergy on transcription during starvationStationary phase is caused by rifampin treatment, and sigma factors block rifampin activity, therebypreventing the onset of stationary phase.Sigma factors create extra nutrients by fixing CO2 and N2 in the air, thereby preventing the onset ofstationary phase.Different sigma factors recognize different promoters. Sigma factors that recognize stress response and catabolicmetabolism promoters are expressed during stationary phase and the housekeeping sigma factor isdownregulated. Thus, transcription shifts toward stress response and away from growth.Sigma factors bind the ribosome and block it from translating certain MRNAS that no longer need to betranslated in stationary phase Sigmas is the stationary phase sigma factor. Which of the following is a likely site for RNAP-SigmaSholoenzyme binding?The terminator region of genes involved in starvation stress responseThe -10 and -35 promoter regions of ribosomal RNA genesThe -10 and -35 promoter regions of genes involved in acid stress responseThe Shine-Delgarno sequence of genes involved in oxidative stress responseThe CAP operator of the lac operon

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Human Anatomy & Physiology (11th Edition)

11th Edition

ISBN:9780134580999

Author:Elaine N. Marieb, Katja N. Hoehn

Publisher:Elaine N. Marieb, Katja N. Hoehn

Chapter1: The Human Body: An Orientation

Section: Chapter Questions

Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...

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Similar questions

LysR regulators like llvY repress transcription from their own promoters. This is called a negative feedback loop. Why might negative feedback be a good way to control expression of a transcriptional repressor? This type of negative feedback loop ensures that ilvC transcription will always be repressed when llvY levels are low, and ilvC will be transcribed highly when llvY levels are high. This type of negative feedback regulation ensures that ilvY is never transcribed. Since llvY is a transcriptional repressor, it will slow down cell growth by blocking transcription. So, llvY represses it's own transcription so that no llvY can ever be made, and the cell can grow. This type of negative feedback loop ensures that there is always a moderate amount of llvY. When IlvY levels fall too low, transcription from the promoter will increase since IlvY won't be able to repress it's own promoter. This negative feedback also ensures that IlVY levels don't rise too high - when llvY levels are high,…
Which of the following is NOT a reason cells regulate gene expression at a level other than the transcriptional level? Some proteins are only required in part of the cell and transcriptional control will only regulate the mRNA/protein throughout the cell. The core promoter for many genes is the same, so these genes will always be transcribed in the same cells. Differential gene expression in different cell types requires regulation of gene expression at levels other than transcription. Transcription and translation are realtively slow processes, so cells need to regulate gene expression post-transcriptionally if they require a fast change in expression of a gene. Not all cells are transcriptionally active (meaning they do not transcribe any genes), so these cells need to regulate gene expression post-transcriptionally.
what is the nature and likely location(s) of a mutant that would, 1)allow constitutive expression of the lac gene? 2)prevent the cell from responding to lactose ( genes are not induced when exposed to lactose)? 3) not allow the cell to utilize lactose even when the genes are induced
You wish to find the cis-acting regulatory DNA elements responsible for the transcriptional responses of two genes, c-fos and globin. Transcription of the c-fos gene is activated in response to fibroblast growth factor (FGF), but it is inhibited by cortisol (Cort). On the other hand, transcription of the globin gene is not affected by either FGF or cortisol, but it is stimulated by the hormone erythropoietin (EP). To find the cis-acting regulatory DNA elements responsible for these transcriptional responses, you use the following clones of the c-fos and globin genes, as well as two “hybrid” combinations (fusion genes), as shown in the diagram below. The letter A represents the intact c-fos gene, D represents the intact globin gene, and B and C represent the c-fos–globin gene fusions. The c-fos and globin exons (E) and introns (I) are numbered. For example, E3(f) is the third exon of the c-fos gene and I2(g) is the second intron of the globin gene. (These labels are provided to help you…
Cell lines divide normally in a defined medium containing growth factors, but fail to divide in the absence AGF (a growth factor). However, a mutant cell line continues to divide even in the absence of AGF. Elevated levels of Rb phosphorylation and the effects of receptor and Mek inhibitors suggest a mutation activating an oncogene. Inhibitors of Mek inhibit cell division of the mutant cell line, but inhibitors to the ADGF receptor, a receptor tyrosine kinase (RTK) with homology to EGFR, do not. Outline the RTK pathway leading to the phosphorylation of Rb to form p-Rb.
The RB (retinoblastoma) protein normally [ Select] ["keep a transcription factor in an inactive state", "keep a transcription factor in an active state", "keep the CDK in a phosphorylated state", "block the function of the APC"] ...But it can be deactivated by [ Select ] ["ubiquitination", "methylation", "phosphorylation", "the use of a GAP"] .Mutations in Rb can lead to cancer because these mutations [ Select ] ["result in constitutive transcription leading to promotion of the cell cycle", "keep CDKs off", "deactivate p53", "increase the production of growth hormones"] PLEASE SELCET THE CORRECT ONE FOR SECTION ONE . EACH SENTECNE HAVE 4 SECTION TO PICK FROM.
Wilms tumor 1, or nephroblastoma, is caused by mutations in the WT1 gene, which encodes a transcription factor. You have identified a novel variant in WT1: Arg422Pro. You have control cells and cells that have been engineered to carry the homozygous WT1 p.Arg422Pro mutation. You want to assess effects of this mutation on a variety of endpoints. For each endpoint listed below, choose the one technique is best suited to answer the question. Choose from: array CGH, qRT-PCR, qPCR, RNA-seq, FISH, in situ hybridization, western blot, immunostaining, WT1 ChIP-seq, WT1 ChIP-PCR, ATAC-seq, 3C Endpoint Technique? WT1 protein amount (quantitative) Western blot WT1 protein binding to all enhancers, genome-wide Chip-seq WT1 mRNA amount (quantitative) WT1 protein subcellular localization Quantitative assessment of all mRNAs in these cells (genome-wide) RNAseq Chromatin interactions between a specific WT1 chromatin binding site (identified above)…
Match each example of mutation to the correct effect on function. Hypomorphic mutation Hypermorphic mutation Antimorphic mutation Neomorphic A deletion results in the loss of part of a protein and the protein retains some of its normal activity. A mutant allele makes a protein with increased cataytic activity. A mutant form of a transcription factor binds new DNA sequences to activate different genes. A mutant from of a receptor protein interferes with the function of the wild-type receptor through heterodimerization.
which is the case only in the context of a robust gene regulator network that maintains the Shh-induced pattern of gene expression
When CAMP binds to the Catabolite Activator Protein (CAP), it causes a conformational change on the protein, which results in binding to the CAP- binding site on the DNA and molecule is known as a(n) of the lac operon. This conformational change induced by the binding of another transcription activation; allosteric effect transcription repression; binding effect translation; distortion effect mutation; interactive effect attenuation; compression effect O O O O
The binding of a small effector molecule, protein-protein interactions, and covalent modifications are three common ways to modulate the activities of transcription factors. Which of these three mechanisms are used by steroid receptors and by the CREB protein?
The Iron Response Factor (IRF) protein regulates production of both the iron transport protein transferrin, which imports iron into a cell, and the iron storage protein ferritin, which stores iron when the cell has more iron than in needs. IRF is an RNA binding protein, which binds to a specific RNA sequence, the Iron Response Element (IRE). When the IRF protein binds to the IRE sequence in the mRNA that codes for transferrin, what effect does this have on the expression of transferrin? Briefly explain why this effect is observed.

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